Sleep fragmentation as an important clinical characteristic of sleep disorders in Parkinson's disease

Cai, Guolong; Luo, Shan; Chen, Lina; Lu, Jianping; Huang, Yujie; Ye, Qinyong

doi:10.1097/cm9.0000000000000329

Cited by 12 publications

(14 citation statements)

References 25 publications

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“…This has revealed that fragmentation appears to be an important component of HD sleep architectural disturbance, including in the premanifest phase. Once again this parallels findings in Alzheimer's and Parkinson's, where sleep fragmentation in particular has been identified as a feature of both premonitory and established disease [62][63][64][65][66].…”

Section: Sleep Architecture Abnormalitiessupporting

confidence: 71%

The sleep and circadian problems of Huntington’s disease: when, why and their importance

2020

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Introduction Mounting evidence supports the existence of an important feedforward cycle between sleep and neurodegeneration, wherein neurodegenerative diseases cause sleep and circadian abnormalities, which in turn exacerbate and accelerate neurodegeneration. If so, sleep therapies bear important potential to slow progression in these diseases. Findings This cycle is challenging to study, as its bidirectional nature renders cause difficult to disentangle from effect. Likewise, well-controlled intervention studies are often impractical in the setting of established neurodegenerative disease. It is this that makes understanding sleep and circadian abnormalities in Huntington’s disease (HD) important: as a monogenic fully penetrant neurodegenerative condition presenting in midlife, it provides a rare opportunity to study sleep and circadian abnormalities longitudinally, prior to and throughout disease manifestation, and in the absence of confounds rendered by age and comorbidities. It also provides potential to trial sleep therapies at a preclinical or early disease stage. Moreover, its monogenic nature facilitates the development of transgenic animal models through which to run parallel pre-clinical studies. HD, therefore, provides a key model condition through which to gain new insights into the sleep-neurodegeneration interface. Conclusions Here, we begin by summarising contemporary knowledge of sleep abnormalities in HD, and consider how well these parallel those of Alzheimer’s and Parkinson’s as more common neurodegenerative conditions. We then discuss what is currently known of the sleep-neurodegeneration cyclical relationship in HD. We conclude by outlining key directions of current and future investigation by which to advance the sleep-neurodegeneration field via studies in HD.

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Section: Sleep Architecture Abnormalitiessupporting

confidence: 71%

The sleep and circadian problems of Huntington’s disease: when, why and their importance

2020

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“…Numerous PSG‐based case–control studies examining sleep in PD have demonstrated distinct changes in each of the different sleep stages 16,17,19,20,22‐24,39‐61 …”

Section: Cortical Electrophysiological Changes In Pd During Sleep — Eegmentioning

confidence: 99%

“…34,36,38 Cortical Electrophysiological Changes in PD During Sleep -EEG Numerous PSG-based case-control studies examining sleep in PD have demonstrated distinct changes in each of the different sleep stages. 16,17,19,20,[22][23][24]…”

Section: Overview Of Normal Sleep Physiologymentioning

confidence: 99%

“…A wide spectrum of sleep disorders have been implicated in PD, encompassing disorders of sleep–wake transition as well as parasomnias involving abnormal movements during various phases of sleep 11‐15 . The most common PD‐associated disturbances in sleep–wake transitioning include increased sleep latency, frequent awakenings, and sleep fragmentation, resulting in wakefulness after sleep onset (WASO) and reduced total sleep time 6,16‐25 . The parasomnias associated with PD have also gained much attention and include rapid eye movement sleep behavior disorder (RBD), periodic limb movements in sleep (PLMS), and restless legs syndrome 12‐14 .…”

mentioning

confidence: 99%

“…[11][12][13][14][15] The most common PD-associated disturbances in sleepwake transitioning include increased sleep latency, frequent awakenings, and sleep fragmentation, resulting in wakefulness after sleep onset (WASO) and reduced total sleep time. 6,[16][17][18][19][20][21][22][23][24][25] The parasomnias associated with PD have also gained much attention and include rapid eye movement sleep behavior disorder (RBD), periodic limb movements in sleep (PLMS), and restless legs syndrome. [12][13][14] Sleep disorders such as RBD can even be the first prodromal symptom of PD prior to the emergence of formal motor symptoms.…”

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confidence: 99%

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The Neurophysiology of Sleep in Parkinson's Disease

et al. 2021

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Sleep disturbances are among the most common nonmotor complications of Parkinson's disease (PD), can present in prodromal stages, and progress with advancing disease. In addition to being a symptom of neurodegeneration, sleep disturbances may also contribute to disease progression. Currently, limited options exist to modulate sleep disturbances in PD. Studying the neurophysiological changes that affect sleep in PD at the cortical and subcortical level may yield new insights into mechanisms for reversal of sleep disruption. In this article, we review cortical and subcortical recording studies of sleep in PD with a particular focus on dissecting reported electrophysiological changes. These studies show that slow-wave sleep and rapid eye movement sleep are both notably disrupted in PD. We further explore the impact of these electrophysiological changes and discuss the potential for targeting sleep via stimulation therapy to modify PD-related motor and nonmotor symptoms.

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Obstructive Sleep Apnea and Striatal Dopamine Availability in Parkinson's Disease

Kim

Lyoo

et al. 2023

Movement Disorders

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A BS TRACT: Background: Sleep disorders are frequently associated with Parkinson's disease. Obstructive sleep apnea syndrome is one of these sleep disorders and is associated with the severity of motor symptoms in Parkinson's disease. Obstructive sleep apnea can lead to dopaminergic neuronal cell degeneration and may impair the clearance of α-synuclein in Parkinson's disease. Striatal dopamine uptake is a surrogate marker of nigral dopaminergic cell damage. Objective: We aimed to investigate the differences in striatal dopamine availability between Parkinson's disease patients with or without obstructive sleep apnea. Methods: A total of 85 de novo and nonmedicated Parkinson's disease patients were enrolled. Full-night polysomnography was performed for all patients, and obstructive sleep apnea was diagnosed as apnea/ hypopnea index ≥5. Positron emission tomography was performed with 18 F-N-(3-fluoropropyl)-2β-carbon ethoxy-3β-(4-iodophenyl) nortropane, and the regional standardized-uptake values were analyzed using a volume-of-interest template and compared between groups with or without obstructive sleep apnea. Results: Dopamine availability in the caudate nucleus of the obstructive sleep apnea group was significantly lower than that of the nonobstructive sleep apnea group. On subgroup analysis, such association was found in female but not in male patients. In other structures (putamen, globus pallidus, and thalamus), dopamine availability did not differ between the two groups. Conclusion: This study supports the proposition that obstructive sleep apnea can contribute to reduced striatal dopamine transporter availability in Parkinson's disease. Additional studies are needed to assess the causal association between obstructive sleep apnea and the neurodegenerative process in Parkinson's disease.

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Sleep fragmentation as an important clinical characteristic of sleep disorders in Parkinson's disease

Cited by 12 publications

References 25 publications

The sleep and circadian problems of Huntington’s disease: when, why and their importance

The sleep and circadian problems of Huntington’s disease: when, why and their importance

The Neurophysiology of Sleep in Parkinson's Disease

Obstructive Sleep Apnea and Striatal Dopamine Availability in Parkinson's Disease

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